CD8+ Cancer Research Results

CD8+, CD8+ T cell: Click to Expand ⟱

Source:

Type: T cell

CD8+ T cells are "end effectors" of cancer immunity.
Cytotoxic T cells expressing cell-surface CD8 are the most powerful effectors in the anticancer immune response and form the backbone of current successful cancer immunotherapies.
CD8+ T cells, also known as cytotoxic T lymphocytes (CTLs), play a crucial role in the immune response against cancer. They are responsible for identifying and killing cancer cells that present abnormal antigens, which can arise from mutations or viral infections.

Scientific Papers found: Click to Expand⟱

346-

AgNPs,

RSQ,

Investigating Silver Nanoparticles and Resiquimod as a Local Melanoma Treatment

in-vivo,

Melanoma,

SK-MEL-28

 AgNP (2 mg/kg) and RSQ (25 mg/kg) administration routes used were peri- and intratumora

 mice

in-vivo,

Melanoma,

WM35

ROS↑,
Ca+2↝, disrupt mitochondrial homeostasis of Ca2+
Casp3↑, x2-4
Casp8↑, x2-4
Casp9↑, x4-14
CD4+↑,
CD8+↑,
tumCV↓,
eff↓, NAC, an ROS scavenger, could efficiently protect B16.F10 cells from the cytotoxic effects of Ag+ even when exposed to high concentrations of Ag+ (250 μg/ml)
*toxicity↓, non-toxic in mice as evidenced by: 1) no significant change in weights during the study period and 2) no significant increases in the levels of liver enzymes, (ALP), (AST), and ALT

541-

Akk,

Akkermansia muciniphila as a Next-Generation Probiotic in Modulating Human Metabolic Homeostasis and Disease Progression: A Role Mediated by Gut-Liver-Brain Axes?

Review,

NA,

GutMicro↑,
PD-1↝,
CD8+↑, CD8+ cytotoxic T lymphocytes (CTLs)
IL8↑,

315-

Api,

Apigenin: Selective CK2 inhibitor increases Ikaros expression and improves T cell homeostasis and function in murine pancreatic cancer

vitro+vivo,

PC,

Panc02

 20 uM

CK2↓, Apigenin: Selective CK2 inhibitor
CD4+↑,
CD8+↑,
Ikaros↑, (API) stabilized Ikaros expression and prevented Ikaros downregulation

5629-

Bif,

ProBio,

Gut microbiota shapes cancer immunotherapy responses

Review,

Var,

eff↑, oral administration of Bifidobacterium enhanced the anti-tumor efficacy of PD-L1 inhibitors by promoting dendritic cell (DC) maturation and increasing tumor-specific CD8 + T cell activity.
DCells↑,
CD8+↑,
eff↑, One study analyzing plasma samples from colorectal cancer (CRC) patients treated with ACT and chemotherapy found that responders had significantly higher blood levels of Bifidobacterium, Lactobacillus, and Enterococcus, indicating that the blood micr
AntiTum↑, Inosine, a purine metabolite produced by Akkermansia muciniphila and Bifidobacterium longum, enhances antitumor immunity by inhibiting UBA6 expression in tumor cells,
other↑, Likewise, vitamin B6, synthesized by Lactobacillus acidophilus and Bifidobacterium bifidum, boosts T lymphocyte proliferation and promotes antitumor immunity by stimulating T cell activity
selectivity↑, Additionally, Bifidobacterium preferentially accumulates in tumors . Bifidobacterium, for example, migrates to colonize and enrich CRC tumors198
GutMicro↑, Microbiome analysis revealed enrichment of beneficial bacteria (Bifidobacterium longum, Lachnospiraceae, Ruminococcaceae) and a decline in potentially detrimental species such as Bacteroides.

1205-

Caff,

immuno,

Caffeine-enhanced anti-tumor activity of anti-PD1 monoclonal antibody

in-vivo,

Melanoma,

B16-F10

OS↑,
CD4+↑, increase in infiltration of CD4+ and CD8+ T lymphocytes into the B16F10 melanoma tumors.
CD8+↑,
AntiTum↑,
TNF-α↑, increased intra-tumoral TNF-α and IFN-γ levels
IFN-γ↑, increased intra-tumoral TNF-α and IFN-γ levels

5892-

CAR,

SRF,

Carvacrol potentiates immunity and sorafenib anti-cancer efficacy by targeting HIF-1α/STAT3/ FGL1 pathway: in silico and in vivo study

in-vivo,

HCC,

 male Sprague–Dawley rats.

Hif1a↓, CVR showed an HIF-1α inhibitory potential, which is highly expressed in HCC tissues.
AFP↑, CVR/SOR enhanced liver functions and decreased AFP level.
hepatoP↑, CVR improves liver functions and enhances SOR anti-cancer activity
STAT3↓, CVR/SOR hindered HCC progression by downregulating STAT3, JAK2, and FGL1.
JAK2↓,
*CD8+↑, CVR/SOR induced tumor immunity via increasing CD8+ T cells.
ChemoSen↑, CVR/SOR is a powerful combination for tumor repression and enhancing SOR efficiency in HCC by modulating FGL1
Dose↝, 10 mg/kg SOR by intragastic tube for 6 weeks daily;
angioG↓, CVR improves SOR attenuation efficacy against TAA-induced angiogenesis

5819-

CBD,

The potential role of cannabidiol (CBD) in lung cancer therapy: a systematic review of preclinical and clinical evidence

Review,

Lung,

Apoptosis↑, Mechanistically, CBD induced apoptosis through pathways such as PPAR-γ activation, mitochondrial dysfunction, and oxidative stress.
PPARγ↓,
mtDam↑,
ROS↑, Induced cell death via apoptosis and increased ROS levels.
EMT↓, It inhibited epithelial-to-mesenchymal transition (EMT), downregulated invasive markers, and modulated the tumor microenvironment by enhancing CD8 + T cell and NK cell activity.
CD8+↑,
NK cell↑,
ChemoSen↑, CBD showed synergistic effects with conventional therapies (e.g., cisplatin, radiotherapy) by increasing drug uptake and overcoming resistance.
ATP↓, CBD decreases intracellular ATP and glucose levels
glucose↓,
Ca+2↑, CBD enhances calcium influx (mediated by TRPV2) and elevates p-ERK expression in CIK cells
TRPV2↑,

6030-

CGA,

Chlorogenic acid induces apoptosis, inhibits metastasis and improves antitumor immunity in breast cancer via the NF‑κB signaling pathway

vitro+vivo,

BC,

MDA-MB-231

subcutaneous tumor mouse model of 4T1 cells

in-vitro,

BC,

MDA-MB-453

in-vitro,

Nor,

MCF10

NF-kB↓, reported that chlorogenic acid (CGA), a potent NF‑κB inhibitor derived from coffee, exerted antitumor activity in breast cancer.
AntiTum↑,
tumCV↓, CGA inhibited viability and proliferation in breast cancer cells.
TumCP↓,
Apoptosis↑, CGA significantly induced apoptosis and suppressed migration and invasion in breast cancer cells.
TumCMig↓,
TumCI↓,
EMT↓, CGA markedly impaired the NF‑κB and EMT signaling pathways.
TumCG↓, results revealed that CGA markedly retarded tumor growth and prolonged the survival rate of tumor‑bearing mice.
OS↑,
TumMeta↓, GA inhibited pulmonary metastasis of 4T1 cells by enhancing the proportion of CD4+ and CD8+ T cells in spleens of mice, which indicated an improvement of antitumor immunity.
CD4+↑,
CD8+↑,
Imm↑, CGA suppresses the pulmonary metastasis of breast cancer by enhancing antitumor immunity

1033-

CHr,

Chrysin inhibits hepatocellular carcinoma progression through suppressing programmed death ligand 1 expression

vitro+vivo,

HCC,

 H22 xenograft mouse model

TumCG↓,
CD4+↑, enhanced CD4/CD8-
CD8+↑, enhanced CD4/CD8-
PD-L1↓, chrysin significantly down-regulated the expression of PD-L1 in vivo and in vitro

1601-

Cu,

The copper (II) complex of salicylate phenanthroline induces immunogenic cell death of colorectal cancer cells through inducing endoplasmic reticulum stress

in-vitro,

CRC,

i-CRT↓, Cu(sal)phen induced the release of calreticulin (CRT), adenosine triphosphate (ATP) and high mobility group box 1 (HMGB1), the main molecular markers of ICD (immunogenic cell death)
ICD↑,
i-ATP↓,
i-HMGB1↓,
ER Stress↑, accumulation of ROS and inducing ERS
ROS↑,
DCells↑, promoted the maturation of dendritic cells (DCs)
CD8+↑, and activation of CD8+T cells
IL12↑, secretion of interleukin-12 (IL-12) and interferon-γ (IFN-γ)
IFN-γ↑,
TGF-β↓, while downregulating transforming growth factor-β (TGF-β) levels

451-

CUR,

The effect of Curcumin on multi-level immune checkpoint blockade and T cell dysfunction in head and neck cancer

vitro+vivo,

HNSCC,

SCC15

1, 2, 5, 10, 20, 40 and 80 µM, 1, 3, 6, 12 and 24 h; 50 mg/kg, 6 weeks

vitro+vivo,

HNSCC,

SNU1076

vitro+vivo,

HNSCC,

SNU1041

TumCMig↓,
TumCG↓,
PD-L1↓,
PD-L2↓,
Galectin-9↓,
EMT↓,
T-Cell↑,
TILs↑,
PD-1↓,
TIM-3↓,
CD4+↓,
CD25+↓,
FoxP3+↓,
E-cadherin↑,
CD8+↑,
IFN-γ↑,

1863-

dietFMD,

Chemo,

Effect of fasting on cancer: A narrative review of scientific evidence

Review,

Var,

eff↑, recommend combining prolonged periodic fasting with a standard conventional therapeutic approach to promote cancer‐free survival, treatment efficacy, and reduce side effects in cancer patients.
ChemoSideEff↓, lowered levels of IGF1 and insulin have the potential to protect healthy cells from side effects
ChemoSen↑,
Insulin↓, causes insulin levels to drop and glucagon levels to rise
HDAC↓, Histone deacetylases are inhibited by ketone bodies, which may slow tumor development.
IGF-1↓, FGF21 rises during intermittent fasting, and it plays a vital role in lowering IGF1 levels by inhibiting phosphorylated STAT5 in the liver
STAT5↓,
BG↓, Fasting suppresses glucose, IGF1, insulin, the MAPK pathway, and heme oxygenase 1
MAPK↓,
HO-1↓,
ATG3↑, while increasing many autophagy‐regulating components (Atgs, LC3, Beclin1, p62, Sirt1, and LAMP2).
Beclin-1↑,
p62↑,
SIRT1↑,
LAMP2↑,
OXPHOS↑, Fasting causes cancer cells to release oxidative phosphorylation (OXPHOS) through aerobic glycolysis
ROS↑, which leads to an increase in reactive oxygen species (ROS), p53 activation, DNA damage, and cell death in response to chemotherapy.
P53↑,
DNAdam↑,
TumCD↑,
ATP↑, and causes extracellular ATP accumulation, which inhibits Treg cells and the M2 phenotype while activating CD8+ cytotoxic T cells.
Treg lymp↓,
M2 MC↓,
CD8+↑,
Glycolysis↓, By lowering glucose intake and boosting fatty acid oxidation, fasting can induce a transition from aerobic glycolysis to mitochondrial oxidative phosphorylation in cancerous cells, resulting in increased ROS
GutMicro↑, Fasting has been shown to have a direct impact on the gut microbial community's constitution, function, and interaction with the host, which is the complex and diverse microbial population that lives in the intestine
GutMicro↑, Fasting also reduces the number of potentially harmful Proteobacteria while boosting the levels of Akkermansia muciniphila.
Warburg↓, Fasting generates an anti‐Warburg effect in colon cancer models, which increases oxygen demand but decreases ATP production, indicating an increase in mitochondrial uncoupling.
Dose↝, Those patients fasted for 36 h before treatment and 24 h thereafter, having a total of 350 calories per day. Within 8 days of chemotherapy, no substantial weight loss was recorded, although there was an improvement in quality of life and weariness.

1850-

dietFMD,

Fasting-mimicking diet remodels gut microbiota and suppresses colorectal cancer progression

in-vivo,

CRC,

mice

TumCP↑, FMD cycles effectively suppressed colorectal cancer growth, reduced cell proliferation and angiogenesis, increased tumor-infiltration lymphocytes especially CD8+T cells
angioG↓,
CD8+↑,
GutMicro↑, FMD stimulated protective gut microbiota, especially Lactobacillus.
eff↑, Additionally, FMD synthesizing with anti-PD-1 therapy effectively inhibited CRC progression.

1859-

dietFMD,

Chemo,

Fasting-Mimicking Diet Reduces HO-1 to Promote T Cell-Mediated Tumor Cytotoxicity

in-vitro,

BC,

4T1

in-vivo,

Melanoma,

B16-BL6

mice

CLP↑, combination of chemotherapy and a fasting-mimicking diet (FMD) increases the levels of bone marrow common lymphoid progenitor cells (CLP) and cytotoxic CD8+ tumor-infiltrating lymphocytes (TILs), leading to a major delay in breast cancer and melanoma
CD8+↑,
TumCG↓,
HO-1↓, In breast tumors, this effect is partially mediated by the down-regulation of the stress-responsive enzyme heme oxygenase-1 (HO-1)
TILs↑, FMD in combination with doxorubicin (DXR) promotes accumulation of tumor-infiltrating lymphocytes (TILs) in the tumor bed

1841-

dietFMD,

Fasting-Mimicking Diet Is Safe and Reshapes Metabolism and Antitumor Immunity in Patients with Cancer

Trial,

Var,

BG↓, In 101 patients, the FMD was safe, feasible, and resulted in a consistent decrease of blood glucose and growth factor concentration
AntiCan↑, mediate fasting/FMD anticancer effects in preclinical experiments
IFN-γ↑, enrichment of IFNγ
eff↑, Cyclic FMD Is Safe in Combination with Standard Anticancer Treatments
Dose↝, five-day FMD followed by 16 to 23 days of refeeding
CD14↓, end of five-day FMD, we found a significant decrease of total monocytes (CD14+)
IGF-1↓, Preclinical evidence in tumor-bearing mice suggests that fasting/FMD-induced reduction of blood glucose and insulin/IGF1 concentration
IGFR↓, induced reduction of serum IGF1 levels is associated with the downregulation of total and activated IGF1R at the tumor level
CD8+↑, where five-day fasting/FMD in patients with breast cancer increased total and activated intratumor CD8+ T cells, aDCs, NK cells, and Tem cells,
NK cell↑,

5070-

dietSTF,

A review of fasting effects on the response of cancer to chemotherapy

Review,

Var,

chemoP↑, Studies suggest that fasting before or during chemotherapy may induce differential stress resistance, reducing the adverse effects of chemotherapy and enhancing the efficacy of drugs.
ChemoSen↑,
*DNArepair↑, (1) repairing DNA damage in normal tissues (but not tumor cells);
*Apoptosis↓, preventing apoptosis-mediated damage to normal cells;
*CD8+↑, depleting regulatory T cells and improving the stimulation of CD8 cells;
UPR↑, accumulating unfolded proteins and protecting cancer cells from immune surveillance
eff↝, discuss how ‘fasting-mimicking diet’ as a modified form of fasting enables patients to eat a low calorie, low protein, and low sugar diet while achieving similar metabolic outcomes of fasting.
TumAuto↑, upregulating autophagy flux as a protection against damage to organelles and some cancer cells;

1283-

GA,

immuno,

Gallic acid induces T-helper-1-like Treg cells and strengthens immune checkpoint blockade efficacy

vitro+vivo,

CRC,

p‑STAT3↓,
Treg lymp↓,
FOXP3↓,
CD8+↑,
IFN-γ↑,

1959-

GamB,

Gambogic acid induces GSDME dependent pyroptotic signaling pathway via ROS/P53/Mitochondria/Caspase-3 in ovarian cancer cells

in-vitro,

Ovarian,

in-vivo,

NA,

mice

AntiCan↑, Gambogic acid (GA) is a naturally active compound extracted from the Garcinia hanburyi with various anticancer activities.
Pyro↑, This study revealed that GA treatment reduced cell viability by inducing pyroptosis in OC cell lines
tumCV?,
CellMemb↓, loss of cell membrane integrity
cl‑Casp3↑, Cleaved caspase-3 and GSDME-N levels increased after GA treatment
GSDME-N↑,
ROS?, GA significantly increased reactive oxygen species (ROS) and p53 phosphorylation.
p‑P53↑,
eff↓, OC cells pretreated with ROS inhibitor N-Acetylcysteine (NAC) and the specific p53 inhibitor pifithrin-μ could completely reverse the pyroptosis post-treatment.
MMP↓, Elevated p53 and phosphorylated p53 reduced mitochondrial membrane potential (MMP) and Bcl-2
Bcl-2↓,
BAX↑,
mtDam↑, damage mitochondria by releasing cytochrome c to activate the downstream pyroptosis pathway
Cyt‑c↑,
TumCG↓, inhibited tumor growth in ID8 tumor-bearing mice
CD4+↑, high-dose GA increased in tumor-infiltrating lymphocytes CD3, CD4, and CD8 were detected in tumor tissues
CD8+↑,

2505-

H2,

Hydrogen gas restores exhausted CD8+ T cells in patients with advanced colorectal cancer to improve prognosis

Trial,

CRC,

55 patients with histologically and clinically diagnosed stage IV colorectal carcinoma were enrolled between July 2014 and July 2017

PGC-1α↑, hydrogen gas was recently reported to activate PGC‑1α,
Dose↝, hydrogen gas for 3 h/day at their own homes and received chemotherapy
CD8+↑, Notably, hydrogen gas decreased the abundance of exhausted terminal PD‑1+ CD8+ T cells, increased that of active terminal PD‑1‑ CD8+ T cells, and improved PFS and OS times,
OS↑,

2504-

H2,

Hydrogen gas activates coenzyme Q10 to restore exhausted CD8+ T cells, especially PD-1+Tim3+terminal CD8+ T cells, leading to better nivolumab outcomes in patients with lung cancer

Trial,

Lung,

A total of 42 of 56 patients with lung cancer treated with nivolumab received hydrogen gas

CD8+↑, As previously reported, hydrogen gas improves the prognosis of patients with cancer by restoring exhausted CD8+ T cells into active CD8+ T cells
OS↑, Median survival time (MST) for the HGN-treated patients was 28 months, a length that is approximately 3-fold longer than that for NO-treated patients (MST 9 months)
eff↝, (PDT+ ratio and CoQ10 ratio, respectively) revealed that patients with low PDT+ ratio (<0.81) and high CoQ10 ratio (>1.175) had significantly longer OS compared with those with high PDT+ ratio and low CoQ10 ratio
CoQ10↑, Hydrogen gas has been suggested to enhance the clinical efficacy of nivolumab by increasing CoQ10 (mitochondria) to reduce PDT+, with PDT+ and CoQ10 as reliable negative and positive biomarkers of nivolumab, respectively.
PDT+↓,
PGC-1α↑, As hydrogen gas is reported to activate PGC1-α (14), it is also one of the mitochondrial activation mediators.
Dose↝, Patients were continuously treated with nivolumab (1 mg/kg) every 2 weeks. Patients also inhaled hydrogen gas 3 h daily at their home through a cannula or mask that they rented or purchased and connected to a Hycellvator ET 100
*toxicity∅, Recently, hydrogen gas inhalation was used in patients with post-cardiac arrest syndrome, and adverse events were not observed

1021-

HNK,

Honokiol suppress the PD-L1 expression to improve anti-tumor immunity in lung cancer

in-vivo,

Lung,

PD-L1↓, in cells with high PD-L1 expression
T-Cell↑, facilitates T cell killing of tumor cells
CD4+↑,
CD8+↑,
TumCG↓, mice

221-

MFrot,

MF,

Low Frequency Magnetic Fields Enhance Antitumor Immune Response against Mouse H22 Hepatocellular Carcinoma

in-vivo,

Liver,

 0.4T, 7.5Hz

 mice

OS↑,
TumCG↓, inhibit
IL6↓,
GM-CSF↓,
CXCc↓, keratinocyte-derived chemokine (KC)
Macrophages↑,
DCells↑,
CD4+↑,
CD8+↑,
IL12↑,

220-

MFrot,

MF,

Effect of low frequency magnetic fields on melanoma: tumor inhibition and immune modulation

in-vitro,

Melanoma,

B16-F10

 0.4 T, 7.5 Hz

 mouse cell line

OS↑, prolonged the mouse survival rate
DCells↑,
T-Cell↑,
Apoptosis↑,
IL1↑,
IFN-γ↓, most of cytokines were decreased
IL10↑,
TumCG↓, grow slowed
ROS↑, Phagocyte activity, ROS release and interleukin-1β (IL-1β) production were significantly promoted after continuous exposure to 50 Hz LF-MF (1mT)
TumCP↓, LF-MF inhibits the proliferation of B16-F10 cells
TumCCA↑, the S-phase rate was significantly decreased from 40.76% to 37.24% and the G2/M-phase rate was significantly increased from 8.9% to 11.6%
ChrMod↑, Compared with control cells, the treated cells were characterized by the breaking down of chromatin (white arrow) and black granule accumulation (black arrow).
CXCL9↓, in tumor-bearing mice groups, most of cytokines were decreased after LF-MF exposure, including KC, CCL1, IFN-γ, CXCL9, CXCL12, TREM-1, CCL12, IL-1rα and IL-16.
CXCL12↓,
CD4+↑, After LF-MF exposure, the proportions of CD3+, CD3 + CD4+ and CD3 + CD8+ T cells in tumor-bearing mice were increased to 24.0%, 13.28% and 7.46%, respectively
CD8+↑,

198-

MFrot,

MF,

Biological effects of rotating magnetic field: A review from 1969 to 2021

Review,

Var,

AntiCan↑, RMF can inhibit the growth of various types of cancer cells in vitro and in vivo and improve clinical symptoms of patients with advanced cancer.
breath↑, 0.4T, 7Hz RMF was applied to treat 13 advanced non-small cell lung cancer patients (2 h/day, 5 days per week, for 6–10 weeks)
Pain↓, Decreased pleural effusion (2 patients, 15.4%), remission of shortness of breath (5 patients, 38.5%), relief of cancer pain (5 patients, 38.5%), increased appetite (6 patients, 46.2%), improved physical strength (9 patients, 69.2%), regular bowel mov
Appetite↑,
Strength↑,
BowelM↑,
TumMeta↓, The same RMF (2 h/day, for 43 days) can also suppress the growth and metastasis of B16-F10 cells in vivo
TumCCA↑, The up-regulated transcription of miR-34a induced cell proliferation inhibition, cell cycle arrest, and cell senescence by targeting E2F1/E2F3, two members of E2F family which are major regulators of the cell cycle,
ETC↓, 2h exposure) effectively inhibited the growth of two types of cultured brain cancer cells, glioblastoma cells and diffuse intrinsic pontine glioma cells. They found that the mitochondrial electron transport chain was significantly disturbed by RMF,
MMP↓, which caused loss of mitochondrial integrity, decreased mitochondrial carbon flux in cancer cells, and eventual cancer cell death (Sharpe et al., 2021).
TumCD↑,
selectivity↑, same group further reported that the same RMF can also selectively kill cultured human glioblastoma and non-small cell lung cancer cells, and leave normal cells unharmed
ROS↑, Mechanistic studies revealed that RMF can increase the mitochondrial ROS level, which further activated the caspase-3 and disturbed the electron fflow in the respiratory chain pathway in cancer cells. (Helekar et al., 2021).
Casp3↑,
TumCG↓, 0.4T, 7.5Hz RMF (2 h/day, for 5 days) inhibited the growth of mouse melanoma cell line B16–F10 in vitro,
TumCCA↑, and its mechanism involved cell cycle arrest and decomposition of chromatins.
ChrMod↑,
TumMeta↓, (2 h/day, for 43 days) can also suppress the growth and metastasis of B16–F10 cells in vivo,
Imm↑, benefiting from improved immune function, including decreased regulatory T cells, increased T cells, and dendritic cells
DCells↑,
Akt↓, inhibiting the activation of the AKT pathway (Tang et al., 2016). T
OS⇅, 51 women with advanced breast cancer underwent RMF treatment. The results showed that 27 patients among them achieved signicant therapeutic effects, and there were no side-effects
toxicity↓,
QoL↑, 13 advanced non-small cell lung cancer patients the quality of life was improved in different degrees. Median survival and 1-year survival rate was 50% and 100% longer
hepatoP↑, In addition, it seems that the RMF can also attenuate liver damage in mice bearing MCF7 and GIST-T1 cells (Zha et al., 2018)
Pain↓, The results showed that the RMF treatment reduced abdominal pain by 42.9% (9/21), nausea/vomiting by 19.0% (4/21), weight loss by 52.4% (11/21), ongoing blood loss by 9.5% (2/21), improved physical strength by 23.8% (5/21) and sleep quality by 19.0%
Weight↑,
Strength↑,
Sleep↑,
IL6↓, Furthermore, decreased levels of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and keratinocyte-derived chemokine (KC) were observed
CD4+↑, it was discovered that macrophages and dendritic cells were activated, CD4+ T and CD8+ T lymphocytes increased, and the ratio of Th17/Treg was balanced.
CD8+↑,
Ca+2↑, effects of RMF were strongly associated with increased calcium tunnel activity and intracellular Ca2+ level in CNS
radioP↑, These results suggest that RMF may be helpful to alleviate the damage of hematopoietic function caused by radiotherapy and chemotherapy
chemoP↑,
*BMD↑, 0.4T, 8Hz RMF treatment (30min/day, for 30 days) along with calcium supplement, synergistically improved bone density
*AntiAge↑, In 2019, Xu et al. reported that a 4h exposure to a 0.2T, 4Hz RMF delayed the aging of human umbilical vein endothelial cells (HUVEC)
*AMPK↑, Mechanistic research revealed that RMF treatment increased the expression of AMPK while reducing the expression of p21, p53 and mTOR.
*P21↓,
*P53↓,
*mTOR↓,
*OS↑, They also discovered that the RMF (2 h/day, for 6, 10 or 14days) can prolong the health status lifespan of Caenorhabditis elegans.
*β-Endo↑, 0.1–0.8T, 0.33Hz RMF treatment signicantly increased the β-endorphin level in the blood of rabbits and humans (23 times higher than before). Moreover, it decreased serotonin (5-HT) in brains, small intestine tissue and serum of mice.
*5HT↓,

MushShi,

The Effects of Active Hexose Correlated Compound (AHCC) on Levels of CD4+ and CD8+ in Patients with Epithelial Ovarian Cancer or Peritoneal Cancer Receiving Platinum Based Chemotherapy

Human,

Ovarian,

28 patients, 14 patients in each group

CD8+↑, However, CD8+ levels were significantly higher in the AHCC group at the sixth cycle of chemotherapy
Pain↑, Adverse events in terms of nausea and vomiting significantly decreased but muscle pain significantly increased in the AHCC group.

5607-

NaHCO3,

Does Baking Soda Function as a Magic Bullet for Patients With Cancer? A Mini Review

Review,

Var,

AntiCan↑, Sodium Bicarbonate “Kills” Cancer Cells
e-pH↑, The utilization of sodium bicarbonate to neutralize the acidity and increase the tumor pHe might control cancer cells progression
TumMeta↓, Sodium bicarbonate reduces the formation of spontaneous metastases and the rate of lymph node involvement in mouse models of metastatic breast cancer.
TumCI↓, administration of 200 mM bicarbonate to 4-week-old TRAMP mice (weaning at 3 weeks) effectively perturbs the in situ evolution of cancer to a microinvasive disease
TumCG↓, sodium bicarbonate significantly controls tumor growth and improves CD8+ T-cell infiltration.
CD8+↑,
NK cell↑, Natural killer (NK) cell activity is also increased in a B-cell lymphoma mouse model following the systemic administration of a buffer therapy.
Remission↑, began a self-administered course of vitamins, supplements, and 60 g of bicarbonate mixed in water daily. As of this submission, he has remained well with stable tumor for 10 months.
eff↑, Therefore, sodium bicarbonate could be used as an adjuvant therapy to enhance the efficacy of conventional treatments.
ChemoSen↑, Surprisingly, extracellular alkalization induced a 2- to 3-fold increase in the efficacy of doxorubicin
ChemoSen↓, it greatly reduces the efficacy of some weak acidic chemotherapeutics, such as chlorambucil.

5604-

NaHCO3,

Mitochondrial metabolic reprogramming of macrophages and T cells enhances CD47 antibody-engineered oncolytic virus antitumor immunity

vitro+vivo,

Melanoma,

B16-BL6

Six-week-old female BALB/c mice and C57BL/6 J mice

in-vitro,

BC,

4T1

eff↑, identified sodium bicarbonate (NaBi) as the potent metabolic reprogramming agent that enhanced antitumor responses in the acidic TME.
eff↑, NaBi and oAd-αCD47 therapy significantly inhibited tumor growth and produced complete immune control in various tumor-bearing mouse models.
TumMeta↓, suggesting its potential as an effective neoadjuvant treatment for preventing postoperative tumor recurrence and metastasis.
pH↑, NaBi improves the acidity of the TME and activates the CaMKII/CREB/PGC1α mitochondrial biosynthesis signaling pathway
CaMKII ↑,
CREB↑,
PGC-1α↑, NaBi increases the mitochondrial content of T cells and BMDMs by promoting the expression of PGC1α mediated by the Ca2+-CaMKII-CREB signaling pathway in an LA environment
AntiTum↑, oral NaBi enhances the antitumor effect of oAd-αCD47.
Imm↑, We proposed that sodium bicarbonate (NaBi) can act as an immunomodulator to reprogram metabolic disorders of CD8+ T cells and TAMs in an acidic environment.
CD8+↑, Combination therapy remodels the immunosuppressive microenvironment to promote activation of CD8+ T cells and TAMs
TAMS↑,

3092-

RES,

Resveratrol in breast cancer treatment: from cellular effects to molecular mechanisms of action

Review,

BC,

MDA-MB-231

Review,

BC,

MCF-7

TumCP↓, The anticancer mechanisms of RES in regard to breast cancer include the inhibition of cell proliferation, and reduction of cell viability, invasion, and metastasis.
tumCV↓,
TumCI↓,
TumMeta↓,
*antiOx↑, antioxidative, cardioprotective, estrogenic, antiestrogenic, anti-inflammatory, and antitumor properties it has been used against several diseases, including diabetes, neurodegenerative diseases, coronary diseases, pulmonary diseases, arthritis, and
*cardioP↑,
*Inflam↓,
*neuroP↑,
*Keap1↓, RES administration resulted in a downregulation of Keap1 expression, therefore, inducing Nrf2 signaling, and leading to a decrease in oxidative damage
*NRF2↑,
*ROS↓,
p62↓, decrease the severity of rheumatoid arthritis by inducing autophagy via p62 downregulation, decreasing the levels of interleukin-1β (IL-1β) and C-reactive protein as well as mitigating angiopoietin-1 and vascular endothelial growth factor (VEGF) path
IL1β↓,
CRP↓,
VEGF↓,
Bcl-2↓, RES downregulates the levels of Bcl-2, MMP-2, and MMP-9, and induces the phosphorylation of extracellular-signal-regulated kinase (ERK)/p-38 and FOXO4
MMP2↓,
MMP9↓,
FOXO4↓,
POLD1↓, The in vivo experiment involving a xenograft model confirmed the ability of RES to reduce tumor growth via POLD1 downregulation
CK2↓, RES reduces the expression of casein kinase 2 (CK2) and diminishes the viability of MCF-7 cells.
MMP↓, Furthermore, RES impairs mitochondrial membrane potential, enhances ROS generation, and induces apoptosis, impairing BC progression
ROS↑,
Apoptosis↑,
TumCCA↑, RES has the capability of triggering cell cycle arrest at S phase and reducing the number of 4T1 BC cells in G0/G1 phase
Beclin-1↓, RES administration promotes cytotoxicity of DOX against BC cells by downregulating Beclin-1 and subsequently inhibiting autophagy
Ki-67↓, Reducing the Ki-67
ATP↓, RES’s administration is responsible for decreasing ATP production and glucose metabolism in MCF-7 cells.
GlutMet↓,
PFK↓, RES decreased PFK activity, preventing glycolysis and glucose metabolism in BC cells and decreasing cellular growth rate
TGF-β↓, RES (12.5–100 µM) inhibited TGF-β signaling and reduced the expression levels of its downstream targets that include Smad2 and Smad3 and as a result impaired the progression of BC cells.
SMAD2↓,
SMAD3↓,
Vim?, a significant decrease in the levels of vimentin, Snail1 and Slug occurred, while E-cadherin levels increased to suppress EMT and metastasis of BC cells.
Snail↓,
Slug↓,
E-cadherin↑,
EMT↓,
Zeb1↓, a significant decrease in the levels of vimentin, Snail1 and Slug occurred, while E-cadherin levels increased to suppress EMT and metastasis of BC cells.
Fibronectin↓,
IGF-1↓, RES administration (10 and 20 µM) impaired the migration and invasion of BC cells via inhibiting PI3K/Akt and therefore decreasing IGF-1 expression and preventing the upregulation of MMP-2
PI3K↓,
Akt↓,
HO-1↑, The activation of heme oxygenase-1 (HO-1) signaling by RES reduced MMP-9 expression and prevented metastasis of BC cells
eff↑, RES-loaded gold nanoparticles were found to enhance RES’s ability to reduce MMP-9 expression as compared to RES alone
PD-1↓, RES inhibited PD-1 expression to promote CD8+ T cell activity and enhance Th1 immune responses.
CD8+↑,
Th1 response↑,
CSCs↓, RES has the ability to target CSCs in various tumors
RadioS↑, RES in reversing drug resistance and radio resistance.
SIRT1↑, RES administration (12.5–200 µmol/L) promotes sensitivity of BC cells to DOX by increasing Sirtuin 1 (SIRT1) expression
Hif1a↓, downregulating HIF-1α expression, an important factor in enhancing radiosensitivity
mTOR↓, mTOR suppression

3141-

VitC,

High-dose Vitamin C inhibits PD-L1 expression by activating AMPK in colorectal cancer

in-vitro,

CRC,

HCT116

Glycolysis↓, Vitamin C inhibits immune evasion by regulating glycolysis
eff↑, VitC suppresses tumor growth and enhances immunotherapy in combination with anti-PD-L1
PD-L1↓, We found that VitC inhibits aerobic glycolysis in HCT116 cells while also downregulating PD-L1 expression.
AMPK↑, VitC's activation of AMPK, which downregulates HK2 and NF-κB, ultimately resulting in reduced PD-L1 expression and increased T cell infiltration.
HK2↓,
NF-kB↓,
Warburg↓, Our research shows that high-dose VitC downregulating the Warburg effect, suppressing CRC growth
tumCV↓, After treatment with VitC, the cell viability of HCT116 cells significantly decreased
GLUT1↓, marked reduction in the mRNA level of glycolysis-related proteins GLUT1, PKM2, and LDHA
PKM2↓,
LDHA↓,
CD4+↑, Our research shows that high-dose VitC increases CD4+ and CD8+ T cell infiltration in tumor tissues by inhibiting PD-L1
CD8+↑,

Showing Research Papers: 1 to 29 of 29

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 29

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↑, 27,
Total Targets: 177

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, Keap1↓, 1, NRF2↑, 1, ROS↓, 1,

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,

Cell Death ⓘ

Apoptosis↓, 1,

DNA Damage & Repair ⓘ

DNArepair↑, 1, P53↓, 1,

Cell Cycle & Senescence ⓘ

P21↓, 1,

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,

Migration ⓘ

β-Endo↑, 1,

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,

Synaptic & Neurotransmission ⓘ

5HT↓, 1,

Clinical Biomarkers ⓘ

BMD↑, 1,

Functional Outcomes ⓘ

AntiAge↑, 1, cardioP↑, 1, neuroP↑, 1, OS↑, 1, toxicity↓, 1, toxicity∅, 1,

Infection & Microbiome ⓘ

CD8+↑, 2,
Total Targets: 21

Scientific Paper Hit Count for: CD8+, CD8+ T cell

4 diet FMD Fasting Mimicking Diet
3 Magnetic Field Rotating
3 Magnetic Fields
2 immunotherapy
2 Chemotherapy
2 Hydrogen Gas
2 Bicarbonate(Sodium)
1 Silver-NanoParticles
1 Resiquimod
1 Akkermansia
1 Apigenin (mainly Parsley)
1 Bifidobacterium
1 probiotics
1 Caffeine
1 Carvacrol
1 Sorafenib (brand name Nexavar)
1 Cannabidiol
1 Chlorogenic acid
1 Chrysin
1 Copper and Cu NanoParticles
1 Curcumin
1 diet Short Term Fasting
1 Gallic acid
1 Gambogic Acid
1 Honokiol
1 Mushroom Shiitake, AHCC
1 Resveratrol
1 Vitamin C (Ascorbic Acid)

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:344  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

CD8+ Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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